Toxicology and applied pharmacology, 2021-11, Vol.431, p.115733, Article 115733
2021
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- Autor(en) / Beteiligte
- Titel
- Amentoflavone prevents ox-LDL-induced lipid accumulation by suppressing the PPARγ/CD36 signal pathway
- Ist Teil von
- Toxicology and applied pharmacology, 2021-11, Vol.431, p.115733, Article 115733
- Ort / Verlag
- United States: Elsevier Inc
- Erscheinungsjahr
- 2021
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- The formation of fat-laden foam cells plays an important role in the initiation and progression of atherosclerosis (AS). Amentoflavone (AF) is found in various traditional Chinese medicines, such as ginkgo biloba, which are used to treat cardiovascular diseases (CVDs). We aimed to explore the potential effects and mechanisms of AF on lipid accumulation, and its possible application in atherosclerotic cardiovascular disease (ASCVD). Cellular models of lipid accumulation were established by treatment of HUASMCs and THP-1 cells with oxidized low-density lipoprotein (ox-LDL). Cell viability, lipid accumulation, and ox-LDL uptake were assessed. Small interfering RNAs (siRNAs) and overexpression plasmids were used to reveal the hierarchical correlations of regulatory pathways. AF reduced the lipid accumulation and ox-LDL uptake induced by ox-LDL, and reduced the expression levels of cluster of differentiation 36 (CD36) and peroxisome proliferator-activated receptor gamma (PPARγ) proteins, while the expression level of ATP binding cassette subfamily A member 1 (ABCA1) increased. Knockdown of PPARγ or CD36 with siRNAs prevented ox-LDL-induced lipid accumulation. Overexpression of CD36 or PPARγ promoted the lipid accumulation induced by ox-LDL and eliminated the effect of AF on ox-LDL-induced lipid accumulation. Overall, AF prevents ox-LDL-induced lipid accumulation by suppressing the PPARγ/CD36 signaling pathway. •Amentoflavone prevents oxidized low-density lipoprotein-induced lipid accumulation.•Amentoflavone prevents oxidized low-density lipoprotein uptake.•Amentoflavone exerts these effects by suppressing PPARγ/CD36 signaling.•Amentoflavone upregulated ABCA1 expression in low-density lipoprotein-induced HUASMCs.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0041-008XeISSN: 1096-0333DOI: 10.1016/j.taap.2021.115733Titel-ID: cdi_crossref_primary_10_1016_j_taap_2021_115733
- Format
- –
- Schlagworte
- Amentoflavone, Atherosclerosis, Atherosclerosis - genetics, Atherosclerosis - metabolism, Atherosclerosis - pathology, Atherosclerosis - prevention & control, ATP Binding Cassette Transporter 1 - metabolism, Biflavonoids - pharmacology, CD36, CD36 Antigens - genetics, CD36 Antigens - metabolism, Foam Cells - drug effects, Foam Cells - metabolism, Foam Cells - pathology, Humans, Hypolipidemic Agents - pharmacology, Lipid Metabolism - drug effects, Lipoproteins, LDL - toxicity, Muscle, Smooth, Vascular - drug effects, Muscle, Smooth, Vascular - metabolism, Muscle, Smooth, Vascular - pathology, Myocytes, Smooth Muscle - drug effects, Myocytes, Smooth Muscle - metabolism, Myocytes, Smooth Muscle - pathology, Ox-LDL, Plaque, Atherosclerotic, PPAR gamma - genetics, PPAR gamma - metabolism, PPARγ, Signal Transduction, THP-1 Cells